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ICAM‐3 (CD50) cross‐linking augments signaling in CD3‐activated peripheral human T lymphocytes
Author(s) -
Berney Seth Mark,
Schaan Tonya,
Alexander J. Steven,
Peterman Gary,
Hoffman Patricia A.,
Wolf Robert E.,
Heyde Henri,
Atkinson T. Prescott
Publication year - 1999
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.65.6.867
Subject(s) - biology , microbiology and biotechnology , icam 1 , peripheral , signal transduction , immunology , cell adhesion molecule , medicine
ICAM‐3 is a pan‐hematopoietic, constitutive adhesion molecule. ICAM‐3 binds to LFA‐1 on antigen‐presenting cells (APC) stabilizing the T cell‐APC interaction, facilitating signaling through the CD3/TCR complex. However, recent evidence using cultured and transformed T cells suggests ICAM‐3 may also function in signaling. Because ICAM‐3 is constitutively expressed on resting T cells, we postulated that signaling through ICAM‐3 in resting T cells represents an important costimulatory mechanism in these cells. In purified resting human T cells, cross‐linking both ICAM‐3 and CD3 with plate‐bound antibodies resulted in a marked increase in cell size (consistent with blastogenesis), synergistically increased surface expression of CD25 and CD69, and increased T cell metabolism. Similarly, concomitant ICAM‐3 and CD3 stimulation significantly ( P < 0.001) increased resting human T cell phosphatidylinositol hydrolysis and phospholipase C‐γ1 phosphorylation. These results indicate that ICAM‐3 augments signaling through CD3, functioning as a costimulatory molecule for resting T cells in the initial activation step. J. Leukoc. Biol. 65: 867–874; 1999.